Dude, I actually compete in powerlifting and I am trying to get my Elite total in the 275 pound weight class in the USPF. My routine is fine and my diet is fine as well. I am just looking for an advantage without ordering illegal steroids through the internet. I have these three drugs and want to know what peoples experience is with any f them run solo as it pertains to strngth without too much weight gain and bloat.If you're concerned about strength only, you must consider and strength training routine and another diet.
In my experience m-drol would be the route to go. Most ppl retain little to no water on this compound, and the strength gains are sic. weight gain due to increase in lbm will still exist, but they should all be very dry.
If you're concerned about strength only, you must consider and strength training routine and another diet.
Dude, I actually compete in powerlifting and I am trying to get my Elite total in the 275 pound weight class in the USPF. My routine is fine and my diet is fine as well. I am just looking for an advantage without ordering illegal steroids through the internet. I have these three drugs and want to know what peoples experience is with any f them run solo as it pertains to strngth without too much weight gain and bloat.
It is when someone is trying to stay in a weight class.That doesn't mean you know sh*t. Don't give me that 'look at me i'm my badest person in the world' bs. I'm telling you that your 'high protein' diet isn't optimal for powerlifting.
It is when someone is trying to stay in a weight class.
Excess carbs do get stored as fat... are you going to try to argue that?
DISCUSSION
We compared the response of liver and adipose tissue lipogenesis to acute and chronic stimulation by carbohydrate ingestion. Hepatic lipogenesis was, in agreement with previous studies (7, 8, 31) clearly responsive to both acute and chronic stimulation while adipose tissue DNL appeared on the contrary poorly responsive. This conclusion is based on several lines of
evidence. First, although oral glucose ingestion in study 2 prevented the decrease in both FAS and SREBP1c mRNA concentrations observed in study 1 there was no increase in these concentrations, as well as in ACC1 mRNA value. This strongly suggests that the expression of lipogenic genes, and presumably the activity of the corresponding proteins, were only
minimally stimulated in adipose tissue by the 12 hour rise in plasma insulin and glucose.
Measurements of proteins amounts and enzyme activity were precluded by the small amount of adipose tissue obtained by needle biopsy. However, there is no shortterm regulation of FAS activity and changes in activity are linked to changes in mRNA level (32). With respect to SREBP1c, the present evidence is that its main regulation is at the transcriptional level and that its activation by proteolytic cleavage is probably a constitutive, nonregulated process (33). The present in vivo result contrasts with in vitro studies showing a stimulation of FAS expression and activity by insulin in human adipocytes (12). Second, FAS, ACC1 and SREBP1c mRNA levels were not increased, but rather decreased, during the high energy high carboydrate diet suggesting strongly that the lipogenic pathway was not stimulated in adipose tissue by carbohydrate overfeeding. Third, these results are consistent with the tracer14 derived estimates of adipose tissue lipogenesis we obtained. The comparaison of deuteriumband 13C enrichments in plasma and adipose tissue TAG clearly shows that adipose tissue lipogenesis was active under the three situations studied. The lack of detectable enrichment in 13C of adipose TAG does not exclude that some uptake of TAGFA occured but shows that this uptake, if present, is low and does not contribute to the deuterium enrichment measured inbadipose TAG. There was, however, no stimulation of lipogenesis in adipose tissue by acute glucose oral load and only a non significant trend for higher lipogenic rate after chronic carbohydrate overfeeding. As a result adipose tissue lipogenesis which was quantitatively comparable to liver lipogenesis in the absence of stimulation (study 1) became less important during either acute or chronic stimulation by carbohydrate feeding. Overall our results agree with those of previous studies which used the incorpation in adipose tissue lipids of 14C from glucose to estimate lipogenesis (4, 5, 15, 34).
We think thus that the stimulation of adipose tissue lipogenesis by massive carbohydrate overfeeding suggested by the study of Aarsland et al (8) is, if real, present only during such extreme, unphysiological situation. The regulation of adipose tissue lipogenesis appears thus different in human beings compared with some other mammalian species. In rats for example adipose tissue lipogenesis is more active and is, as liver lipogenesis, responsive to high insulin/glucose levels and to variations of carbohydrate intake (35, 36). SREBP1c plays a major role in the regulation of lipogenic genes expression, at least in their response to insulin (18, 37, 38). This transcription factor is a major determinant of the lipogenic capacity of mammalian and avian tissues (39). Therefore it is possible that SREBP1c expression is low in human adipose tissue, compared to other species, but such comparison between human beings and other species has not been performed to our knowledge. The lack of response in our study of adipose tissue FAS and ACC1 expression and lipogenesis to acute or chronic carbohydrates overfeeding could be related to the lack of increase of SREBP1c mRNA. Since SREBP1c expression is stimulated in rats by dietary carbohydrates and/or insulin (18, 40, 41) it would remain to determine why this stimulation is absent in human adipose tissue.
The comparison of the quantitative estimate of hepatic and adipose lipogenesis during study 2 with the amount of glucose ingested (less than 1g vs 250270g) shows that the
contribution of this metabolic pathway to the disposal of ingested glucose was minimal. The increase of hepatic and adipose lipogenesis after an hypercaloric high carbohydrate diet (11.5 g/day) was also moderate and can thus explain only a minimal part the weight gain of the
subjects (1500g in average during the two weeks of controled diet). Since liver biopsies for measurement of tracer incorporation in liver TAG were not performed for obvious ethical reasons we cannot exclude the possibility that some newly synthesized fatty acids remained within liver TAG stores. However, it seems very unlikely that an increase in liver TAG stores
could explain a large part of the disposal of ingested glucose in study 2 and of the weight gain observed during the high energy high carbohydrate diet. An increase in lipogenesis in another tissue is unlikely. Therefore the most probable explanations for the observed body weight
increase are merely a repletion of muscles and liver glycogen stores, along with the simultaneous storage of water, and the suppression of fat oxidation leading to the deposition of ingested fat. Moreover, altough the contribution of fat to total energy intake was decreased during the high energy, high carbohydrate diet, the total amount ingested was increased.
In conclusion, our results show that in normal humans adipose tissue lipogenesis, although active, is quantitatively a minor pathway and is less responsive than hepatic lipogensis to acute or prolonged carbohydrate overfeeding. The picture could be different in obesity but the recent finding that lipogenic genes expression is decreased in adipose tissue of obese subjects (11) makes this possibility unprobable. Thus, DNL in adipose tissue is an unlikely contributor to the development of dietary induced obesity in humans.
I would rather eat more protein than carbs. It works for me so I might as well keep doing it. My macros are about 50-25-25. I feel good eating like this. I ate this way while taking h-drol and bold and I gained a considerable amount of strength-and kept those gains after PCT. I only gained about 8 pounds. I would like to try a different compound this time around. I wish M-DHT were still around because that stuff made me very aggressive and strong., but didnt put any weight on me.How so? Let me guess you think carbohydrates are stored as fat?
when weight comes on that fast, its not muscle. Its rapid uptake of water and glycogen puffing out the muscles. Its not keepable by itself, but it allows your muscles to work way harder and get way stronger, and its in the ensuing days that actual muscle is built. thought i should clarify that.
This is exactly what happens with creatine, but most people dont know that. They think the creatine is building the muscle but its not, it only allows you to lift a little bit heavier and train a little bit longer which in turn will make you grow faster.
So let me get this straight, your claiming that a study group was fed 150% of their bmr requirement and that the extra 50% kcals were CHO and they gained 4g a day...
Adipose DNL is active in humans, but contributes little to TAG stores and is less responsive than liver DNL to stimulation by carbohydrates.
In conclusion, the lipogenic capacity of adipose tissue is lower in humans than in rats. This is not related to differences in diet and is probably explained by lower abundance of SREBP-1c protein. A decreased expression of ChREBP could also play a role.
DNL has a relatively high energetic cost and its importance in total triglyceride balance continues to be debated. At most, DNL is thought to contribute minimally to total body lipid stores.
Even at the highest measured levels (7 g/d), the amount of fat synthesized is minor relative to the average daily adult consumption of fat, which is 50–150 g.
De novo lipogenesis did not differ significantly between lean and obese subjects, except with the control treatment, for which de novo lipogenesis was greater in the obese subjects. De novo lipogenesis was 2- to 3-fold higher after overfeeding by 50% than after the control treatment in all subjects. The type of carbohydrate overfeeding (sucrose or glucose) had no significant effect on de novo lipogenesis in either subject group. Estimated amounts of absolute VLDL production ranged from a minimum of 2 g/d (control) to a maximum of 10 g/d after overfeeding.
Wow. I understand the concept and have looked into it b4 but the part that caught me off guard was that the were taking in 150% of their BMR requirements. That is WAY more kcals than needed. I would have figured that given sufficent insulin (and seeing that the extra 50% was CHO, I'm sure there is), that would be enough kcals to increase adipose tissue significantly no matter what macro it was. I would like to know how they figured their BMR though. If just useing one of the many calculators, and not experimenting themselves to find their true BMR, theresults would be badly skewed. The formulas are usually quite a bit off. Does it say in the study if there is a controll group takeing 100% of their BMR useing the same formula to figure it?
But, did it mention if there was a controll group? I'd like to talke a look at that study if you can pm it to me. Im intrigued.
the orignal study you posted about. 150% of bmr kcals with little weight gain.
I'm pretty sure if he's totaling elite in the 275s, he's got his sh1t together.That doesn't mean you know sh*t. Don't give me that 'look at me i'm my badest person in the world' bs. I'm telling you that your 'high protein' diet isn't optimal for powerlifting.
I had the exact same results. By the end of my 2nd week of pplex, I was so bloated I felt like my fingers were going to explode when I closed my fists. I hated phera. I'm at the end of the epi portion of the bridge now, and I'm not noticing much strength-wise other than my normal strength curve. And yes my diet is dialed in.I'd stay away from the Pheraplex based upon what you seem to be looking for. I just stopped an Epistane/Pheraplex cycle early because the Pheraplex was wreaking havoc with me. I gained about 16 lbs in 4 weeks and it seems like it is mostly h20 weight. I'm puffy and bloated and that was not really what I was looking for when I decided to stack the Phera w/ Epi. With me, the Pheraplex appears to be a sopping wet designer. My back pumps were so bad from the Phera, all of my compound lifts went down and it got hard to even complete a workout.
I'm pretty sure if he's totaling elite in the 275s, he's got his sh1t together.
Haha, do you know what elite is?
An Elite total in the 275 weight class is 1,946. I totaled just under 1900 at a meet in April and my p.r's add up to 1,920. The 1802 was done completely drug free and I am determined to get this elite total at my next meet. I am not obese, but def, not shredded. (not shredded, not concerned!).No. I'm a complete idiot, please explain. Do you know what internet exaggeration is? Anyone can claim anything. Maybe he is, maybe he isn't. Maybe he knows a lot, maybe he doesn't. Just because someone weighs 275 doesn't make them an expert.
An Elite total in the 275 weight class is 1,946. I totaled just under 1900 at a meet in April and my p.r's add up to 1,920. The 1802 was done completely drug free and I am determined to get this elite total at my next meet. I am not obese, but def, not shredded. (not shredded, not concerned!).